Coag exam review

what is virchows triad

1. components of blood

2. vessel structure

3. blood flow

endothelium prevents clots

• secreting substances to keep plt from sticking

• makes thrombomodulin

• released t-pa

• heparan sulfate

first response to injury

vasoconstriction

damaged endothelium is clot inducing

• exposure of collagen receptors to trigger plt adhesion

• TXA2 released to activate plts

• Weibel-palade bodies release vWF

• Tissue factor is released

• PAI- 1,2,3,4 released to limit fibrinolysis

Plt maturation sequence

1. megakaryoblast

2. promegakaryocyte

3. megakaryocyte

4. Plt

life span of plt is

7-10 days

what organ holds 1/3 of all plts

spleen

normal range of plts

150-400 ×10³

what are the 4 zones of plts

• peripheral

• structural

• organelle zone

• membranous

peripheral zone is

the outer part of the plt F3

structural zone manages

the shape changeand aggregation of platelets.

organelle zone manages

the release of granules

The membranous zone manages the

chemicals released from the plt

Alpha granules contain

• PF4

• PDGF

• Beta thromboglobulin

• coag factors

dense bodies contain

• storage pool ADP and Ca+

• serotonin

PDGF does what

starts wound repair

PF4 does what

neutralizes heparin

Beta thromboglobulin

neutralizes heparin

What is the process of aggregation

1. collagen is exposed on endothelial

2. vWF binds subendothelium

3. plt binds to GP1b/IX (adhesion)

4. exposing GPIIb/IIIa on plts and chemicals released from granules (activation)

5. These receptors bind fibrinogen which creates a plt to plt bridges (aggregation)

A stimulating chemical is called a

agonist

Dense bodies release

ADP and Ca+

AP binds to plt membrane, activates enzymes releasing…

Arachidonic acid

The next enzyme released after arachidonic acid is

cyclooxygenase

cyclooxygenase converts arahidonic acid to

Thromboxane A2

What does thromboxane A2 do

amplifies aggregation

What inactivates thromboxane A2 throught the binding of arachidonic acid

ASA, Aspirin

bleeding due to plts primary first step

family history is first step

primary hemostasis symptoms

• epistaxis

• mucous membranes

• external skin

How to screen for primary hemostasis

plt function, plt count

what are 4 primary hemostasis disorders

• hereditary hemorrhagic telangiatasia

• osteogenesis imperfecta

• Marfans

• Ehlers danlos

what is a common defect in primary hemostasis disorders

abnormal or no collagen leading to no plt adhesion

low plts is

thrombocytopenia

decreased production of plts is seen in

• aplastic

• myelophthisic

• acute leukemia

• myelodysplastic

• megaloblastic anemia

• chemotherapy/radiation

Acute ITP is in what populaion

kids post viral

How is acute ITP treated

it usually self resolves in 1 month to 6 weeks

Chronic ITP is in what population

women of child bearing age

what is the treatment for chronic ITP

steroids and splenectomy

HIT antibodies are made against

Plt factor 4 complex

Non immune mechanisms that cause destruction of plts are

• TTP

• HUS

• DIC

TTP is triggered by what and what are the coag tests results?

• AdamsTS13 deficiency

• normal PT, aPTT and D-Dimer

HUS is triggered by what and what are the coag tests results?

• e.coli infection

• normal PT, PTT, ad D-dimer

DIC is triggered by what and what are the coag tests results?

• sepsis, OB complications, leukemia or trauma

• prolonged PT, aPTT and elevated D-dimer

What shows abnormal with Epi but normal with ADP

aspirin is present

What shows a abnormal epi and ADP?

von willibrands disease or bernard solier or plavicks syndrome or platelet function defects.

what test is used for P2Y12 ADP inhibition

Verify Now

Glanzmanns thrombasthenia defect

2b-3a receptor

Bernard-Soulier syndrome defect

1b9 receptor

von willebrands disease defect is

von willebrands factor

storage pool disorders (including aspirin) defect

lack of granule release

Plt aggregation results for Bernard-Soulier Syndrome abnormal results in

Ristocetin and Ristocetin/normal plasma as it's missing the 1b9 receptor on the plt

Plt aggregation results for von willebrands disease abnormal results are

only ristocetin because the factor is added back into the mix during the mixing study

plt aggregation results for Glanzmanns that are abnormal

• ADP (flat lines)

• Epinephrine

• collagen

  

Plt aggregation results for storage pool disorders and aspirin

APD- normal

Epinephrine- normal

Collagen- normal

Ristocetin- normal

Arachidonic acid- abnormal

Extrinsic factor uses what factors and test

7, 10, 5,2,1

PT

Intrinsic factors uses what factors and what test

12,11,9,8,10,5,2,1

PTT

Common pathway uses what factors and test

10,5,2,1

PT/PTT

Contact factors

12, 11,HMWK, prekalikrein

Vit K dependent factors

2,7,9,10

Fibrinogen group cofactors

8,5,fibrinogen, 13

Process of fibrinogen to fibrin

1. cleavage of A and B fibrinopeptides

2. fibrin monomer is formed

3. fibrin monomers polymerize

4. F13 and ca+ creates cross links

Secondary hemostasis shows bleeding symptoms in what way

deep tissue bleeding and bleeding in the joints

deficiencies in clotting proteins are known as

hemophilias

inheritance pattern for vWF

Dominant

inheritance for 8 and 9 def.

x-linked

how do blood groups play a roll in VW disease

type O has lower amounts and type A and B have high amounts

vW factor binds to

Plt GP1B/IX and promotes adhesion to subendothelial collagen

how does VW disease affect secondary hemostasis

it complexs with factor 8, 1:1, extending factor 8’s half life

vonwillebrands disease is tested for via what tests

• ADAMSTS-13

• vWF multimer analysis

• vWF activity

• antigen

what is the treatment for VW disease

DVADP nose spray

hemophilia A

fator 8 def.

hemophilia B

factor 9 def.

severe hemophilia is

1% or less of factor

moderate hemophilia

1-6% of fractor

Mild hemophilia

6-40% of factor

Treatment to X-linked hemophilias

recombinant factor

inhibitors in X linked hemophilia

Factor9 autoantibodies

contact factors in recessive disorders are what and have what symptoms

11,12, prekalikrein, HMWK

have no bleeding

hemophilia C is a deficiency in

Factor 11

Parahemophilia has a deficiency

factor 5 deficiency

what are the recessive hemophilia disorders

• contact factors

• hemophilia C

• parahemophilia

• fibrinogendef. /dysfibrinogen

• factor 13

severe hemophilia has what symptoms

• spontaneous joint bleeding

• spontaneous deep tissue/brain bleed

moderate hemophilia has what symptoms

• bleeding at circumcision

• excess bleeding after surgery and minor injuries

mild hemophilia symptoms

often goes undetected until excess bleeding after surgery

if a specimen is underfilled what would the PT be

long

over filled specimen for PT

short/increase in clots

hemolyzed samples have a

short PT/PTT

patients with hct of >55% have a

long PT/PTT

clotted samples have a

>100 PT and >200 PTT

how do you store a sample for coag

double spin to remove plts; freeze in -70C

Prothrombin time reagents

• thromboplastin (TF/Cl2)

• CaCl2

sources for prothrombin

• human brain/placenta

• rabbit brain

• recombinant

sensitivity of prothrombin time measured by

ISI

• closer to 1 is more sensitive

Protime used to monitor

coumadin

what is the specimen stability for a PT

24hrs

What is the therapeutic range for INR

2-3

What is the bedside version of PT

whole blood INR

PTT measures what pathway

intrinsic

what are the reagents for PTT

• PTT reagent (phospholipids/ativators)

• CaCl

What is the stability of PTT and why

4hrs because the plt neutralize PF4

PTT is used to screen

any factor but 7